Editorial: Exercise-induced neuroplasticity in neurodegeneration diseases, volume II

Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and related disorders, represent an escalating global health challenge. As life expectancy increases, the burden of chronic neurological conditions continues to rise (Imam et al., 2025). Despite extensive research efforts, the development of effective pharmacological disease-modifying therapies remains limited. As a result, growing attention has been directed toward non-pharmacological strategies aimed at preventing, delaying, or mitigating neurodegeneration. Among such strategies, exercise has emerged as one of the most promising interventions due to its capacity to modulate neuroplasticitythe brain's intrinsic ability to reorganize and adapt through changes in structure, function, and connectivity (Erickson et al., 2011;Northey et al., 2018).Exercise-induced neuroplasticity encompasses a broad spectrum of adaptive mechanisms, including synaptic remodeling, angiogenesis, mitochondrial biogenesis, and enhanced neurogenesis within brain regions critical for cognition and motor control (Liang et al., 2021;Lu et al., 2023;Zhang et al., 2024). These neurobiological adaptations contribute to improved neural efficiency, resilience, and repair, counteracting pathological processes such as oxidative stress, neuroinflammation, and protein aggregation that characterize neurodegenerative disorders (Li et al., 2024;Lu et al., 2023;Sun et al., 2022). Recent evidence suggests that the beneficial effects of exercise extend beyond cellular and molecular levels to encompass network-level plasticity, facilitating improved communication among distributed brain regions (Dimitriadis et al., 2024;Rosso et al., 2025;Yu et al., 2024;Zhang et al., 2022). Such findings position exercise not only as a therapeutic tool for symptom management but also as a potential modifier of disease progression.